Profile of Cognitive Impairment in Parkinson's Disease
Identifieur interne : 000579 ( Main/Exploration ); précédent : 000578; suivant : 000580Profile of Cognitive Impairment in Parkinson's Disease
Auteurs : G. Stennis Watson [États-Unis] ; James B. Leverenz [États-Unis]Source :
- Brain Pathology [ 1015-6305 ] ; 2010-05.
English descriptors
Abstract
Cognitive impairment (CI) is a common nonmotor complication of Parkinson's disease (PD), and is associated with significant disability for patients and burden for caregivers. Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy‐related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease‐specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.
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DOI: 10.1111/j.1750-3639.2010.00373.x
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Similar to motor symptoms, the characteristics of CI in PD can be quite variable, both in terms of what cognitive domains are impaired, and the timing of onset and rate of progression. This review will examine the profile of cognitive domain impairments observed in PD, with a focus on early CI (without dementia). We will also discuss possible relationships between specific cognitive domain impairments in PD and pathological processes such as Lewy‐related pathology and Alzheimer's disease. It is our hypothesis that the specific characteristics of CI observed in individual PD patients provide clues to the underlying pathological processes, and that understanding the biological basis of this clinical phenomenon will assist in directing disease‐specific treatments. Given the high lifetime risk for CI in PD, it is imperative that we improve our understanding and treatments for this common and disabling problem in PD.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Watson, G Stennis" sort="Watson, G Stennis" uniqKey="Watson G" first="G. Stennis" last="Watson">G. Stennis Watson</name></region><name sortKey="Leverenz, James B" sort="Leverenz, James B" uniqKey="Leverenz J" first="James B." last="Leverenz">James B. Leverenz</name><name sortKey="Watson, G Stennis" sort="Watson, G Stennis" uniqKey="Watson G" first="G. Stennis" last="Watson">G. Stennis Watson</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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